PUBLICATION

Effect of acute exposure of saxitoxin on development of zebrafish embryos (Danio rerio)

Authors
Chen, G., Jia, Z., Wang, L., Hu, T.
ID
ZDB-PUB-200422-27
Date
2020
Source
Environmental research   185: 109432 (Journal)
Registered Authors
Keywords
Angiogenesis, Apoptosis, Reactive oxygen species, Saxitoxin, Zebrafish
MeSH Terms
  • Animals
  • Apoptosis
  • Embryo, Nonmammalian
  • Oxidative Stress
  • Reactive Oxygen Species
  • Saxitoxin/toxicity
  • Water Pollutants, Chemical*/toxicity
  • Zebrafish*
PubMed
32247151 Full text @ Environ. Res.
Abstract
As a type of cyanobacterial toxins, saxitoxin (STX) is receiving great interest due to its increasing presence in waterbodies. However, the underlying mechanism of STX-induced adverse effect is poorly understood. Here, we examined the developmental toxicity and molecular mechanism induced by STX using zebrafish embryos as an animal model. The embryonic toxicity induced by STX was demonstrated by inhibition of embryo hatching, increase in mortality rate, abnormal heart rate, abnormalities in embryo morphology as well as defects in angiogenesis and common cardinal vein remodeling. STX induced embryonic DNA damage and cell apoptosis, which would be alleviated by antioxidant N-acetyl-L-cysteine. Additionally, STX significantly increased reactive oxygen species level, catalase activity and malondialdehyde content and decreased the activity of superoxide dismutase and glutathione content. STX also promoted the expression of vascular development-related genes DLL4 and VEGFC, and inhibited VEGFA expression. Furthermore, STX altered the transcriptional regulation of apoptosis-related genes (BAX, BCL-2, P53 and CASPASE 3). Taken together, STX induced adverse effect on development of zebrafish embryos, which might be associated with oxidative stress-induced apoptosis.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping